A review of current and future medical therapies for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

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✓In an effort to help clarify the current state of medical therapy for cerebral vasospasm, the authors reviewed the relevant literature on the established medical therapies used for cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH), and they discuss burgeoning areas of investigation. Despite advances in the treatment of aneurysmal SAH, cerebral vasospasm remains a common complication and has been correlated with a 1.5- to threefold increase in death during the first 2 weeks after hemorrhage. A number of medical, pharmacological, and surgical therapies are currently in use or being investigated in an attempt to reverse cerebral vasospasm, but only a few have proven to be useful. Although much has been elucidated regarding its pathophysiology, the treatment of cerebral vasospasm remains a dilemma. Although a poor understanding of SAH-induced cerebral vasospasm pathophysiology has, to date, hampered the development of therapeutic interventions, current research efforts promise the eventual production of new medical therapies.

Abbreviations used in this paper:CAM = cell adhesion molecule; CBF = cerebral blood flow; eNOS = endothelial nitric oxide synthase; ET = endothelin; NXY-059 = disodium 2,4-disulfophenyl-N-tert-butylnitrone; SAH = subarachnoid hemorrhage.

✓In an effort to help clarify the current state of medical therapy for cerebral vasospasm, the authors reviewed the relevant literature on the established medical therapies used for cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH), and they discuss burgeoning areas of investigation. Despite advances in the treatment of aneurysmal SAH, cerebral vasospasm remains a common complication and has been correlated with a 1.5- to threefold increase in death during the first 2 weeks after hemorrhage. A number of medical, pharmacological, and surgical therapies are currently in use or being investigated in an attempt to reverse cerebral vasospasm, but only a few have proven to be useful. Although much has been elucidated regarding its pathophysiology, the treatment of cerebral vasospasm remains a dilemma. Although a poor understanding of SAH-induced cerebral vasospasm pathophysiology has, to date, hampered the development of therapeutic interventions, current research efforts promise the eventual production of new medical therapies.

Abbreviations used in this paper:CAM = cell adhesion molecule; CBF = cerebral blood flow; eNOS = endothelial nitric oxide synthase; ET = endothelin; NXY-059 = disodium 2,4-disulfophenyl-N-tert-butylnitrone; SAH = subarachnoid hemorrhage.

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Contributor Notes

Address reprint requests to: E. Sander Connolly Jr., M.D., Columbia University College of Physicians and Surgeons, 710 West 168th Street, Room 435, New York, New York 10032. email: esc5@columbia.edu.

© AANS, except where prohibited by US copyright law.

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